ArticleRespiratory research2018
IL-32γ attenuates airway fibrosis by modulating the integrin-FAK signaling pathway in fibroblasts.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Deleted in lymphocytic leukemia 2 contributes to lung fibroblast activation and pulmonary fibrosis by interacting with and triggering focal adhesion kinase phosphorylation.Respiratory research · 2026Article
- Integrins and pulmonary fibrosis: Pathogenic roles and therapeutic opportunities.Biomolecules & biomedicine · 2025Review
- Interleukin-32: a Pandora's box in human immunodeficiency virus infection.Frontiers in immunology · 2025Review
- Pre-metastatic niche: formation, characteristics and therapeutic implication.Signal transduction and targeted therapy · 2024Review
- Bronchial Asthma, Airway Remodeling and Lung Fibrosis as Successive Steps of One Process.International journal of molecular sciences · 2023Review
- Mechanosensitive Piezo1 channels mediate renal fibrosis.JCI insight · 2022Article
- Pathobiology of Airway Remodeling in Asthma: The Emerging Role of Integrins.Journal of asthma and allergy · 2022Review
- The Combined Model of CX3CR1-Related Immune Infiltration Genes to Evaluate the Prognosis of Idiopathic Pulmonary Fibrosis.Frontiers in immunology · 2022Article
- Focusing on Mechanoregulation Axis in Fibrosis: Sensing, Transduction and Effecting.Frontiers in molecular biosciences · 2022Review
- Macrophage-Secreted S100A4 Supports Breast Cancer Metastasis by Remodeling the Extracellular Matrix in the Premetastatic Niche.BioMed research international · 2022Article
- Role of interleukins in the pathogenesis of pulmonary fibrosis.Cell death discovery · 2021Review
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundFibrosis in severe asthma often leads to irreversible organ dysfunction. However, the mechanism that regulates fibrosis remains poorly understood. Interleukin (IL)-32 plays a role in several chronic inflammatory diseases, including severe asthma. In this study, we investigated whether IL-32 is involved in fibrosis progression in the lungs.
methodsMurine models of chronic airway inflammation induced by ovalbumin and Aspergillus melleus protease and bleomycin-induced pulmonary fibrosis were employed. We evaluated the degree of tissue fibrosis after treatment with recombinant IL-32γ (rIL-32γ). Expression of fibronectin and α-smooth muscle actin (α-SMA) was examined and the transforming growth factor (TGF)-β-related signaling pathways was evaluated in activated human lung fibroblasts (MRC-5 cells) treated with rIL-32γ.
resultsrIL-32γ significantly attenuated collagen deposition and α-SMA production in both mouse models. rIL-32γ inhibited the production of fibronectin and α-SMA in MRC-5 cells stimulated with TGF-β. Additionally, rIL-32γ suppressed activation of the integrin-FAK-paxillin signaling axis but had no effect on the Smad and non-Smad signaling pathways. rIL-32γ localized outside of MRC-5 cells and inhibited the interaction between integrins and the extracellular matrix without directly binding to intracellular FAK and paxillin.
conclusionsThese results demonstrate that IL-32γ has anti-fibrotic effects and is a novel target for preventing fibrosis.
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